Meal-induced increases in parasympathetic and sympathetic activity elicit simultaneous rises in plasma insulin and free fatty acids

Steffens, A.B.; Gugten, Jan van der; Gödeke, Julia; Luiten, P.G.M.; Strubbe, J.H.

doi:10.1016/0031-9384(86)90393-8

Cited by 53 publications

(23 citation statements)

References 13 publications

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“…For example, during insulininduced hypoglycemia, both the SNS and PNS are activated (Havel & Taborsky, 1989). Similarly, oral sensory stimulation also elicits both PNS and SNS activity (Diamond & LeBlanc, 1987;LeBlanc & Cabanac, 1989;Steffens et al, 1986). Each of the cells within the pancreatic islet is differentially sensitive to neural stimulation.…”

Section: Innervation Of the Endocrine Pancreas Innervation Of The Endmentioning

confidence: 96%

Nutritional implications of the cephalic-phase reflexes: endocrine responses

2000

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Section: Innervation Of the Endocrine Pancreas Innervation Of The Endmentioning

confidence: 96%

Nutritional implications of the cephalic-phase reflexes: endocrine responses

2000

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“…This pathway relies on the autonomic system (Buijs & Kaalsbeck, 2001), either through its neuronal projections or through adrenal hormonal release. Previous studies in rats by Steffens et al (1986) reported increased blood levels of epinephrine (EPI) and norepinephrine (NE) during the first 5 min after a meal, followed by an increase of insulin and glucose. Similar results were reported by LeBlanc and Cabanac (1989) in human patients, indicating an immediate activation of the sympathetic system elicited by food ingestion.…”

Section: Introductionmentioning

confidence: 99%

Daily Epinephrine but not Norepinephrine Administration Produces Anticipatory Drinking Behavior in Rats

Mendoza¹,

Aguilar‐Roblero²,

Dı́az-Muñoz³

et al. 2003

Biological Rhythm Research

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Peripheral oscillators, especially in the liver, are thought to be part of the food entrained oscillator (FEO). The internal mediating signals involved in food entrainment are unknown. Catecholamines may be one signal, since they increase their blood concentration immediately after feeding, and their intraperitoneal (IP) administration produces hyperglycemia and a satiety response by their direct effect on the liver. The present study explored the role of epinephrine (EPI) and norepinephrine (NE) as entraining signals to the FEO. This effect was explored by daily IP administration of EPI (12.5 mg/100 g bw), NE (25 mg/100 g b) or vehicle on rhythmicity of drinking behavior in rats maintained under constant conditions. Behavioral effects were compared with those observed in a group entrained with a restricted feeding schedule (RFS). IP administration of EPI produced anticipatory drinking behavior, in a dosedependent manner but with a lower intensity than that produced by RFS. In contrast, daily NE or vehicle administration did not produce any changes in drinking rhythmicity. None of the manipulations produced effects on the SCN-dependent freerunning period. Present data suggest a role of EPI as a factor involved with the internal mediating signal for FEO; however, other preabsortive or postabsortive signals may also be part of this complex entraining pathway.

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“…54 Sympathetic activation may further reinforce the increase in FFA by promoting lipolysis 55 -57 or by decreasing FFA utilization and their re-esterification. 58 There are several postulated mechanisms by which FFA may elevate arterial pressure. 61 FFA may also lead to insulin resistance, 62 as discussed below.…”

Section: Possible Mechanisms Of Obesity-induced Hypertensionmentioning

confidence: 99%

Pathways from obesity to hypertension: from the perspective of a vicious triangle

et al. 2002

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Obesity and arterial hypertension are important public health problems. Both overweight and hypertension predispose to cardiovascular diseases, such as myocardial infarction, stroke and renal failure. Moreover, overweight clearly predisposes to hypertension, and thus to an increased prevalence of cardiovascular diseases. This in turn favors inactivity and further weight gain, leading to an exacerbation of cardiovascular disorders. Obesity, hypertension and cardiovascular diseases thus contribute to three corners of a vicious triangle. It is within this conceptual framework that this paper reviews the pathogenesis of obesityrelated hypertension, which is highly complex. Many factors act together to promote vasoconstriction and sodium retention. Leptin, free fatty acids and insulin, whose levels are increased in obesity, may act synergistically to stimulate sympathetic activity and vasoconstriction. In addition, obesity-induced insulin resistance and endothelial dysfunction may operate as amplifiers of the vasoconstrictor response. Finally, increased renal tubular reabsorption of sodium may also occur, caused by an increased renal sympathetic nerve activity, the direct effect of insulin, hyperactivity of the renin -angiotensin system and possibly by an alteration of intrarenal physical forces. All together, these factors will lead to sustained hypertension. Because the prevalence of obesity was steadily increasing in the last decades, leading to an increased prevalence of hypertension and cardiovascular disorders, obesity and hypertension will most likely become the health challenges of the twenty-first century.

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Meal-induced increases in parasympathetic and sympathetic activity elicit simultaneous rises in plasma insulin and free fatty acids

Cited by 53 publications

References 13 publications

Nutritional implications of the cephalic-phase reflexes: endocrine responses

Nutritional implications of the cephalic-phase reflexes: endocrine responses

Daily Epinephrine but not Norepinephrine Administration Produces Anticipatory Drinking Behavior in Rats

Pathways from obesity to hypertension: from the perspective of a vicious triangle

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